It has been a relatively short time between clinical use of the term anxiety neurosis—which included worry, panic, and obsessions—and the advent of recent DSM-defined categorical diagnoses of panic disorder, generalized anxiety disorder, social anxiety disorder, posttraumatic stress disorder, and obsessive-compulsive disorder. It seems that we have moved from a symptom-oriented approach in treating anxiety to a syndromal approach in which the patient has to accumulate enough symptoms and impairment to have a more definable illness or disorder.

The merits of the DSM system are abundant. We have research-based criteria that aid in accurate diagnoses of many mental illnesses. This psychiatric diagnostic system, if used correctly, is probably more sensitive and specific than any other medical specialty’s approach to systematic diagnosis. An accurate diagnosis makes it possible to study disease-specific treatments that are likely to afford better outcomes for our patients. The DSM approach has allowed us access to more randomized controlled trials and ultimately more FDA-approved psychotropic medications. This has allowed for many more early intervention approaches with more benign medications and has probably helped alleviate the symptoms of mental illness in more patients than was possible just a few decades ago.

Others would argue that DSM is flawed and difficult to work with. Patients are not a list of symptoms, and some patients do not fit into specific categories. Furthermore, many patients have comorbid mental illnesses. This is a problematic issue because most psychotherapies, and all FDA-approved medications, are not well studied in comorbid populations.

At times it feels as though categorizing these illnesses has been immensely helpful in promoting psychiatric research and patient care. At the same time, though, we have the “forest” at the expense of the “tree” effect where individual patients have unique symptoms that do not “fit,” or where we do not have an adequate evidence base from which to choose treatments. This may leave some patients undertreated or only partially responsive to treatment.

We psychiatrists are now employing terms that oncologists use. For example, we want our patients to be in “remission,” which is a relative absence of symptoms and a return to premorbid psychosocial functioning. When FDA-approved medications and manualized therapies fail to bring about remission, we must go “off-label” and use integrative or eclectic psychotherapies or medications that have not been fully studied.

We could reverse our syndromal approach and go back to working on key target symptoms, (eg, worry, sadness, executive dysfunction). Psychotherapies such as cognitive-behavioral therapy (CBT) are focused on alleviating key distressing symptoms. For example, panic can be treated with CBT whether the panic is generated by social anxiety, posttraumatic anxiety, or is driven by panic disorder itself. From a biological perspective, we could use the work of Stephen Stahl1 and deconstruct syndromes into symptoms as described in the most recent edition of his psychopharmacology textbook or in his many peer-reviewed articles. Stahl suggests that if a patient has a psychiatric symptom, (eg, inattention), then he or she might have this as part of a larger syndrome (eg, attention-deficit disorder, major depressive disorder, or generalized anxiety disorder).

Even though these 3 DSM disorders or syndromes are unique and present differently, from the brain’s point of view inattention is inattention. It is possible that all of these patients with different DSM disorders have abnormal processing on a transmitter/receptor level (serotonin), or even on a brain circuitry and neuroanatomy level where the cortex is poorly communicating with the anterior cingulates and with limbic structures. An imbalance in this complex circuitry may cause inattention, regardless of the phenotypically noticeable full set of DSM signs and symptoms associated with the DSM disorder. Using this theory, the choice of medication for symptom-specific inattention may be based on using those that alter the malfunctioning circuit (which causes a single symptom)—and not on a medication that treats a full disorder.

In the future, treating anxiety is likely to continue to be a top-down approach in which syndromes are treated with manualized, well- studied psychotherapies and FDA-approved medications that will lead to complete response in our patients. To gain full remission, we must think and proceed differently. We must conduct more studies that focus on treating comorbidities, and we must aggressively treat residual independent symptoms in a bottom-up approach which is symptom-based, not syndrome-based. I feel that many of the articles included in this Special Report offer something unique in these areas and may be directly applicable to patient care.